Sudden sensorineural hearing loss (SSNHL) was first described by De Kleyn in 1944 and is defined as a hearing loss of at least 30 dB over three contiguous audiometric frequencies and occurs within three days or less [1]. Its incidence is 5−20 cases per 100,000 people and affects men and women equally. SSNHL is more common in patients aged 50−60 years [2-4]. There are various reasons for SSNHL occurrence including infections, trauma, tumors, autoimmune diseases, ototoxic drugs, and metabolic/neurologic diseases [5]; however, theoretically, the main reasons are: viral infections, vascular blockage, cochlear membrane disruption, and autoimmune diseases. In many cases, SSNHL is classified as “idiopathic” [6].

In SSNHL, hearing loss is often accompanied by tinnitus in 70−90% of cases and vertigo as 20−70% [7,8]. Vertigo is mostly found in patients with profound hearing loss and hearing improvement in patients with accompanying vertigo tends to be less than those without any vertigo [9]. The close proximity of vestibule to cochlea causes simultaneous vertigo and hearing loss (especially in high frequency). In this way, cochlear damage is transmitted to vestibular organs through ductus reunions [10]. There are different treatment options for SSNHL, including high dose oral steroids, antiviral drugs, steroids combined with antivirals or vasodilators, anticoagulants, vitamin B complex, benzodiazepine, magnesium, plasma expanders, carbogen inhalation, hyperbaric oxygen and intratympanic steroids. Steroid therapy is the most acceptable method among others [11]. Corticosteroids can lead to the improvement of inner ear inflammation; they are mostly given by mouth rather than by injection [4]. Cervical vestibular evoked myogenic potential (cVEMP) is an inhibitory electro muscular response recorded from the ipsilateral sternocleidomastoid (SCM) via sound, vibration, and electrical stimulation.

It is a saccular-originated response with a positive peak at a mean latency of 13 ms (p13) and a negative trough at 23 ms (n23). The video head impulse test (vHIT) is a relatively new objective and fast diagnostic method for the evaluation of semi-circular canal function through vestibulo-ocular reflex (VOR) [12,13]. By assuming the involvement of vestibular and nervous systems in SSNHL and considering the necessity of residual vestibular function evaluation (as a latent problem) in these patients before and after steroid therapy as the conventional treatment. The aim of the present study was to evaluate the results of cVEMP and vHIT used for assessment of superior and inferior vestibular nerves in saccule and semi-circular canals in patients with SSNHL before and after steroid treatment.

METHODS

The study was performed at the Department of ENT Government medical college Doda. It was a comparative cross-sectional study conducted on 23 subjects with monaural sudden sensorineural hearing loss (SSNHL) (9 females and 14 males; mean age, 38 ± 11.69 years). They were selected using convenience sampling technique from among patients referred to the ENT department from January 2023 to July 2023. The inclusion criteria were: age < 60 years; referral to clinic within one week after SSNHL onset; no other diseases that can cause vertigo and vestibular problems such as diabetes and vascular compression syndrome, regardless of having vertigo or not; cervical pain; limited cervical movement (according to the patients and test results); and no disease in middle ear. Exclusion criteria included were lack of patient cooperation, neck pain during vHIT, and nausea or vomiting during vHIT. After obtaining written consent from subjects and evaluation of inclusion criteria, the following tests were performed: otoscopy, tympanometry and pure tone audiometry air conduction (AC) and bone conduction (BC) at octave frequencies from 250 to 8000 Hz. Patients with mild to profound hearing loss were included in the study. The cVEMP was recorded by Bio-logic Navigator Pro (Germany). The electrode array comprised the non-inverting on the middle part of SCM, inverting on the upper part of sternum, and the ground on forehead. For contracting SCM, patients were positioned supine with head turned to the opposite side. Stimuli were delivered through inserting earphone to the ipsilateral ear. Stimulation had following characteristics: 500 Hz tone burst (2 ms rise/fall time and 0 ms plateau), rarefaction polarity, 95 dB nHL stimulation level (5 per second), 5000 gains, filtering between 10−1000 Hz, 50−100 ms time window, and 150 sweeps. To test the repeatability of the response, each intensity level of response was tested twice after a rest. To seek threshold, the test was started at 95 dB nHL and Intensity was decreased in 5 dB steps. The lowest level in which a repeatable response was recorded, was defined as threshold. This process was repeated for the second ear as well [14]. The vHIT was performed by ICS Head Impulse (GN Otometrics, Denmark). The goggle was put on the patients and the test process was explained to them. Patients were asked to look at the point on the wall from a 1 m distance. After calibration, for testing lateral semi-circular canal, the tester put her hands on the patient’s head and performed 10 fast impulse movements (at least 100 degrees per second) with 5−20 degrees to the sides. After each impulse, head remained in the last position to avoid masking any covert saccades. The timing and direction of impulses were different to avoid prediction [15]. After a rest, the stimulation of posterior and anterior semicircular canals was performed. For right posterior and left superior semi-circular canals, patient’s head was turned 45 degrees to the right with one hand on top of the head and the other beneath the chin. After a rest, stimulation of left posterior and right superior semicircular canals was performed by turning head 45 degrees to the left. Each stage was performed twice. Steroid therapy was given at 1mg/kg prednisolone every morning with an oral omeprazole every 12 hours for 10 days. If hearing was not improved after 10 days, intratympanic injection of 4mg/mL dexamethasone twice a week for two weeks was prescribed (a total of four injections given in supine position with the head 45 degrees turned to the unaffected side). After one month, all procedures were performed again for all patients. Kolmogorov-Smirnov test results showed that all collected data had normal distribution. Then, paired t-test was used for comparing quantitative parameters of cVEMP and VOR gain in normal and abnormal ears before and after treatment and comparing the mean of these parameters before and after treatment between two ears. McNemar’s test was used for comparing the cVEMP incidence ratio in each ear before and after treatment and between ears before and after treatment. All analyses were performed in SPSS 16 software.

RESULTS

Table 1 presents the distribution of SSNHL audiometric configurations before and after steroid therapy. Prior to treatment, a flat audiogram pattern was observed in 60.9% of patients with 43.5% showed severe SSNHL. Following therapy, the greatest recovery rate (13%) was seen in patients with an ascending audiogram configuration and those with mild SSNHL. Figure 1 illustrates the post-treatment changes in audiogram patterns. cVEMP responses were identified in 73.9% of affected ears compared with 100% of unaffected ears at baseline, with a significant interaural difference in response incidence (p = 0.031). After treatment, cVEMP responses were present in all ears. Quantitative cVEMP results are summarized in Table 2. Statistically significant differences were observed in mean p13 latency and p13–n23 amplitude between ears and across pre- and post-treatment stages (p<0.05). In addition, the cVEMP threshold in the affected ear, the interaural difference in mean p13–n23 amplitude before treatment, and the asymmetry ratio between pre- and posttreatment were all significantly different (p < 0.05). Table 3 outlines the mean VOR gain values for each semicircular canal. Significant differences were found in the posterior canal gain of the unaffected ear before and after treatment, as well as between anterior and posterior canal gains within each ear after therapy (p < 0.05). However, comparisons of VOR gain between ears after treatment revealed no significant difference (p > 0.05).

DISCUSSION

SSNHL frequently involves vestibular dysfunction due to the anatomical and vascular connections between cochlea and vestibule [10,16–19]. In this study, 13% of patients presented with vertigo, which declined to 8.7% after treatment. Reported rates vary widely; Yu and Li observed vertigo in 20–60% of SSNHL cases and emphasized that vestibular impairment can occur even in the absence of vertigo [8]. cVEMP findings demonstrated significant improvement after steroid therapy, with bilateral responses recorded in all patients. Amplitude asymmetry, initially present in 39.1%, decreased to 17.39% post-therapy, indicating partial but not complete recovery of saccular and inferior vestibular nerve function. These results are consistent with earlier reports showing cVEMP abnormalities in 0–77% of SSNHL cases [17,20] and improvement following treatment [21,22]. vHIT analysis showed that VOR gain in the anterior and posterior canals increased significantly after therapy. Before treatment, abnormal VOR gain (<0.7) was noted in 47.82% (posterior) and 30.43% (anterior) of patients; after therapy, this decreased to 8.7% and 13.04%, respectively. Some contralateral abnormalities were also identified, suggesting subclinical vestibular involvement. Our results parallel Pogson et al., who reported posterior canal dysfunction in 74% of SSNHL patients [24], and Yao et al., who showed that posterior canal deficits predominate in SSNHL, whereas vestibular neuritis more often affects all canals [25].

Steroid therapy remains the mainstay of SSNHL management, though its vestibular effects are less well established [26]. Improvements observed in cVEMP and vHIT in our cohort likely reflects recovery of reversible peripheral dysfunction through the anti-inflammatory and vasoactive properties of corticosteroids [26,27].

CONCLUSION

Vestibular dysfunction is common in sudden sensorineural hearing loss (SSNHL), affecting the saccule, semicircular canals, and associated pathways. Steroid therapy improved both auditory and vestibular outcomes, though residual abnormalities persisted in some patients. Comprehensive vestibular evaluation, combined with targeted rehabilitation, may enhance balance recovery in SSNHL.

Conflict of interest: None

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